Peripheral Edema associated with Olanzapine: case report

Introduction Olanzapine is a second generation antipsychotic. Sedation and weight gain are common treatment side effects. However, other rare side effects such as peripheral edema are yet to be documented. Objectives Our study aimed to describe the clinical presentation of edema in a patient taking Olanzapine. Methods Case report Results We present the case of a 42 male patient hospitalized for a manic episode. He was put on Olanzapine at 10 mg a day. During the hospitalization, the patient exhibited profuse pitting edema on his lower limbs and a rapid weight gain. He presented no other physical sign such as a fever, cutaneous lesions or trouble walking. Thrombophlebitis and erysipelas were eliminated after an extensive physical exam, complete blood work and doppler ultrasound exam of both legs. Olanzapine was discontinued and the patient was prescribed a 4-day course of loop diuretics. Complete resolution of symptoms was noted 5 days later. Conclusions Further research regarding the mechanism behind edema in patients taking second generation antipsychotics are needed. We recommend monitoring for edema with initiation and titration of Olanzapine treatment. Disclosure of Interest None Declared

Introduction: Olanzapine is a second generation antipsychotic. Sedation and weight gain are common treatment side effects. However, other rare side effects such as peripheral edema are yet to be documented. Objectives: Our study aimed to describe the clinical presentation of edema in a patient taking Olanzapine. Methods: Case report Results: We present the case of a 42 male patient hospitalized for a manic episode. He was put on Olanzapine at 10 mg a day. During the hospitalization, the patient exhibited profuse pitting edema on his lower limbs and a rapid weight gain. He presented no other physical sign such as a fever, cutaneous lesions or trouble walking. Thrombophlebitis and erysipelas were eliminated after an extensive physical exam, complete blood work and doppler ultrasound exam of both legs. Olanzapine was discontinued and the patient was prescribed a 4-day course of loop diuretics. Complete resolution of symptoms was noted 5 days later. Conclusions: Further research regarding the mechanism behind edema in patients taking second generation antipsychotics are needed. We recommend monitoring for edema with initiation and titration of Olanzapine treatment.

Disclosure of Interest: None Declared
Schizophrenia and other psychotic disorders 01

EPP0102 The Role of Social Defeat in Neurological differences in Psychotic Patients
A. Malaviya 1 *, P. A. Lalousis 1 , S. J. Wood 1 , A. Bertolino 2 , S. B. Borgwardt 3 , P. Brambilla 4 , J. Kambeitz 5 , R. Lencer 6 , C. Pantelis 7 , S. Ruhrmann 8 , R. K. Salokangas 9 , F. Schultze-Lutter 10 , E. Meisenzahl 10 , N. Koutsouleris 11 and R. Upthegrove 1 Introduction: The social defeat hypothesis (SDH) suggests that a chronic experience of social defeat increases the likelihood of the development of psychosis. The SDH indicates that a negative experience of exclusion leads to an increase in the baseline activity of the mesolimbic dopamine system (MDS), which in turn leads to the onset of psychosis. Social defeat models have previously been produced using animal models and preclinical literature; however, these theories have not fully been tested in human clinical samples. There have been studies implying changes in brain structure due to social defeat interactions; however, research evidence is varied.
Objectives: This study aims to uncover whether exposure to SoDe has an impact on brain structure. Furthermore, we hope to understand if these changes are relevant to other mental health disorders. Methods: 698 (506 no SoDe, 191 SoDe) participants between the ages of 15-41 were recruited from the PRONIA-FP7 study. SoDe was measured from the self-reported questionnaires' Bullying Scale' and 'The Everyday Discrimination Scale'. T1-weighted structural MRI data were processed; five 2 sample t-test analyses were carried out to compare the GMV differences in the entire sample and between the four groups. Results: The VBM analysis showed significant group interactions in the right thalamus proper when comparing participants who had experience SoDe to participants who had not experienced SoDe including all 4 groups along with left cerebral white matter differences. In the ROP subgroup, significant group interactions in the left cerebellum white matter were found along with right cerebral white matter, left cerebral white matter and right Thalamus proper. Conclusions: The findings suggest that there are significant group interactions in thalamus and cerebral white matter. This is in keeping with some previous research suggesting volumetric changes in the thalamus due to stress and psychosis. Similarly for white matter there is some evidence suggesting differences due to SoDe and psychosis. However, there is a scarcity of research in this area with different research suggesting distinctive findings and therefore the evidence is inconclusive. In the ROP group analysis significant group interactions were present in the cerebellum due to SoDe experience. There is research suggesting the cerebellum's role in multiple different aspects like social interaction, higher-order cognition, working memory, cognitive flexibility, and psychotic symptoms, with every research suggesting multiple different things the role of the cerebellum in SoDe in the ROP population is in question. Nonetheless this large-scale research presents some interesting novel finding and leads the way to a new area of research. Further analysis will explore the relationship between groups on markers of stress (CRP) and neuroinflammation as potential mediation of the environmental effects of SoDe.

Disclosure of Interest: None Declared
European Psychiatry S183